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I have lordosis which is an over-exaggerated curve in the lumbar spine. My first memories of this were as a teenager when my back would periodically go into spasm. As a child until my mid twenties I danced and I was forever being told not too stick my bum out which is visually what lordosis looks like – your bum sticks out and so does your belly. I have always found flexion (bending) my spine tricky however extending (arching/back-bending) very easy.

Pilates initially made me more body aware. I danced semi-professionally so I have always been body aware but Pilates takes it to another level. I started to learn and understand where my movements were restricted and what I needed to activate or deactivate to get parts to move or not to move in certain positions/directions.

Through Pilates I have learnt to engage my deep abdominals – ever been told to pull in your stomach but not taught how? This was all of my dance career! I am able to pick my pelvis up so I do not over arch my back and I have leant the tools to lengthen my lumbar spine and to flex my spine.

As researchers unravel the molecular machinery that links exercise and cognition, working out is emerging as a promising neurotherapy.

Nov 1, 2018

ASHLEY YEAGER

For an hour a day, five days a week, mice in Hiroshi Maejima’s physiology lab at Hokkaido University in Sapporo, Japan, hit the treadmill. The researcher’s goal in having the animals follow the exercise routine isn’t to measure their muscle mass or endurance. He wants to know how exercise affects their brains.

Researchers have long recognized that exercise sharpens certain cognitive skills. Indeed, Maejima and his colleagues have found that regular physical activity improves mice’s ability to distinguish new objects from ones they’ve seen before. Over the past 20 years, researchers have begun to get at the root of these benefits, with studies pointing to increases in the volume of the hippocampus, development of new neurons, and infiltration of blood vessels into the brain. Now, Maejima and others are starting to home in on the epigenetic mechanisms that drive the neurological changes brought on by physical activity.

In October, Maejima’s team reported that the brains of rodents that ran had greater than normal histone acetylation in the hippocampus, the brain region considered the seat of learning and memory.1 The epigenetic marks resulted in higher expression of Bdnf, the gene for brain-derived neurotrophic factor (BDNF). By supporting the growth and maturation of new nerve cells, BDNF is thought to promote brain health, and higher levels of it correlate with improved cognitive performance in mice and humans.

With a wealth of data on the benefits of working out emerging from animal and human studies, clinicians have begun prescribing exercise to patients with neurodegenerative diseases such as Parkinson’s and Alzheimer’s, as well as to people with other brain disorders, from epilepsy to anxiety. Many clinical trials of exercise interventions for neurodegenerative diseases, depression, and even aging are underway. Promising results could bolster the use of exercise as a neurotherapy.

“No one believes exercise is going to be a magic bullet,” says Kirk Erickson, a cognitive psychologist at the University of Pittsburgh. “But that doesn’t mean we shouldn’t do it.”

The body-brain connection

In the late 1990s, then-postdoc Henriette van Praagand other members of Rusty Gage’s lab at the Salk Institute for Biological Studies in La Jolla, California, were fascinated with recent findings from the group showing that mice whose cages had toys and running wheels developed more new neurons in the hippocampus, a brain area important for learning and memory, than mice living in less-stimulating enclosures.

Van Praag wanted to identify which element of enriched environments had the greatest influence on the brain. She had some mice learn to swim in a water maze, while others swam in open water, ran on a running wheel, or interacted with several other mice. After 12 days, the development of new neurons was greatest in the group of mice that ran: they had double the number of new neurons as mice in the maze or water.2

In a follow-up study published a few months later, van Praag and her colleagues showed that the neurogenesis sparked by running on the wheel correlated with the mice’s ability to remember the location of a hidden platform in a tank of water. The brains of the mice that ran also had greater reorganization of synaptic connections than those from mice that didn’t run, suggesting exercise influences plasticity.3 “The whole line of research into exercise and neurogenesis grew from there,” says van Praag, who started jogging regularly after seeing the results.

Over the past two decades, researchers have identified many molecular mechanisms underlying exercise’s influence on cognition. Exercise, studies have shown, leads to the release of proteins and other molecules from muscle, fat, and liver tissue that can affect levels of BDNF and other agents that spur neurogenesis, speed new-neuron maturation, promote brain vascularization, and even increase the volume of the hippocampus in humans.

3. SPERMIn the sperm of male mice that exercise, the abundance of certain microRNAs associated with learning and memory increases. The mice’s offspring show slight cognitive advantages compared with offspring of sedentary mice.

The question then became: How do these factors change the expression of genes in the brain? In 2009, neuroscientist Hans Reul of the University of Bristol and colleagues published one of the first studies to look broadly for epigenetic changes in response to exercise. The team put rats through a stressful challenge, placing them into new cage environments or forcing them to swim in a beaker of water. After the stressful experiences, animals that had run regularly on a wheel had higher levels of histone acetylation across the genome in cells of the dentate gyrus, a part of the hippocampus where neurogenesis occurs. The active animals then acted less stressed than their more sedentary counterparts when reexposed to the stressful environments. The rats that exercised spent less time exploring the new cage or struggling in the water, where they instead floated with their heads above water. The findings suggest that the acetylation induced by the combination of running and stress helped the animals better cope with subsequent stress.4

Exercise-induced epigenetic changes “have a remarkable capacity to regulate synaptic and cognitive plasticity,” says Fernando Gomez-Pinilla, a neuroscientist at the University of California, Los Angeles, who has led several similar studies.

Since Reul’s study, at least two dozen others have reported acetylation and other epigenetic changes that link exercise to the brain in rodents. Moses Chao, a molecular neurobiologist at the New York University School of Medicine, and colleagues recently found that mice that ran frequently on wheels had higher levels of BDNF and of a ketone that’s a byproduct of fat metabolism released from the liver. Injecting the ketone into the brains of mice that did not run helped to inhibit histone deacetylases and increased Bdnfexpression in the hippocampus. The finding shows how molecules can travel through the blood, cross the blood-brain barrier, and activate or inhibit epigenetic markers in the brain.5

While some researchers probe the epigenetic connection between exercise and cognitive prowess, others continue to unveil previously unknown links. In 2016, for example, van Praag, now at the Florida Atlantic University Brain Institute, and colleagues found that a protein called cathepsin B, which is secreted by muscle cells during physical activity, was required for exercise to spur neurogenesis in mice. In tissue cultures of adult hippocampal neural progenitor cells, cathepsin B boosted the expression of Bdnf and the levels of its protein and enhanced the expression of a gene called doublecortin (DCX), which encodes a protein needed for neural migration. Cathepsin B knockout mice had no change in neurogenesis following exercise.

No one believes exercise is going to be a magic bullet. But that doesn’t mean we shouldn’t do it.—Kirk Erickson, University of Pittsburgh

Van Praag’s team also found that nonhuman primates and humans who ran on treadmills had elevated blood serum levels of cathepsin B after exercising. Following four months of running on the treadmill three days per week for 45 minutes or more, participants drew more-accurate pictures from memory than at the beginning of the study, before they started exercising.6

A handful of research groups have now begun to pains-takingly look for other molecules released during exercise that could enhance the activity of Bdnf and other brain-boosting genes, says van Praag, and it’s becoming clear that what’s happening in the body affects the brain. “We don’t think about that [connection] as much as we should.”

Healing action

Since the 1980s, studies of humans have pointed to a link between exercise and gains in cognitive performance. Understanding this relationship is of particular importance to patients with neurological diseases. University of Southern California neuroscientist Giselle Petzinger has been treating patients with Parkinson’s disease for decades and has observed that those who exercise can improve their balance and gait. Such an observation hinted that the brain retains some plasticity after disease symptoms set in, she says, with neural connections forming to support the gains in motor skills.

A few years ago, Petzinger and her colleagues began studying a mouse model of Parkinson’s disease. The team found that active mice had more dopamine receptors in the basal ganglia, a group of neuronal structures important for movement, learning, and emotion.7 Levels of dopamine receptors correlate with brain plasticity, and dopamine receptor loss is one of the signature signs of Parkinson’s disease. Using a dopamine antagonist as a radioactive tracer, the team found that patients who walked on a treadmill three times per week for eight weeks increased the numbers of dopamine receptors in the basal ganglia.8

Paying it forwardAs early as the 1990s, studies started to show indirect links between pregnant women’s physical activity and the brains of their gestating babies. For example, a 1996 study showed that at age five, children of moms who exercised regularly during pregnancy performed better on tests of general intelligence and oral language skills than children whose mothers had not exercised much (J Pediatrics, 129:856–63). And research backing this association continues to accumulate. In 2016, for instance, one study showed that boys born to physically active mothers had higher scores on math and language tests than boys from sedentary moms (J Matern Fetal Neonatal Med, 29:1414–20).

Scientists have long assumed that the exercise-induced changes to offspring are epigenetic in nature, and recent research is beginning to support that hypothesis. One group reported in 2015 that three months of physical exercise changed the DNA methylation patterns of young men’s sperm. The tweaks occurred at genes associated with schizophrenia, Parkinson’s disease, and other brain disorders (Epigenomics, doi: 10.2217/epi.15.29).See “Ghosts in the Genome”To further investigate exercise-induced changes in gene expression, Anthony Hannan of the Florey Institute of Neuroscience and Mental Health in Victoria, Australia, and colleagues studied the sperm of mice that ran on wheels or performed other physical activities. The team showed that exercise spurred changes in the expression levels of several small RNAs in the germline cells of male mice. It is known that small RNAs packaged into gametes can influence the metabolism of offspring, and possibly also learning and memory. Male mice born to fathers with these changes in their sperm had reduced anxiety levels, leading the authors to conclude that parental exercise can exert a transgenerational effect on offspring’s emotional health (Transl Psychiat, 7:e1114, 2017).

Earlier this year, André Fischer, an experimental neuropathologist at the German Center for Neurodegenerative Diseases in Göttingen, and his colleagues published one of the most convincing studies showing that the benefits of an enriched environment on the brain can be passed epigenetically from parent to offspring. The team put adult male mice in cages with running wheels and other toys, while a set of their cousins lived in cages without wheels or toys. Synaptic connections increased in the mice in enriched environments, and the team also saw increased connections in the brains of the active mice’s offspring—both males and females. The offspring learned a little faster and had a bit better memory recall than mice with parents reared in traditional cages, though the differences were not statistically significant (Cell Rep, 23:P546–54, 2018). Analyzing the sperm of the parent mice, Fischer and his colleagues identified two microRNAs—miR212 and miR132, both associated with the neuron development—that appeared to affect cognitive abilities of the active mice’s offspring.

It’s not yet clear if these findings are translatable to humans, but Fischer and his colleagues write in their study that the results could be important for reproductive medicine. “The idea that . . . training in adulthood provides a cognitive benefit not only to the individual undergoing this procedure, but also to its offspring is fascinating.”

Petzinger’s mouse studies have also revealed other possible mechanisms of exercise’s benefits for Parkinson’s patients, including the maintenance of dendritic spines, the tiny projections that branch off of nerve cells to receive electrical input from other neurons nearby, and of the synapses along these spines.9 These effects appear to modify synaptic connectivity within the mice’s brains and modify the animals’ disease progression, says Petzinger, who is just wrapping up a trial on using exercise to target cognitive impairment in Parkinson’s disease.

Prescription exercise may also be beneficial for Alzheimer’s patients or individuals at risk of developing the disease. Several studies show that physical activity can counter the elevated risk of developing the disease among individuals carrying the APOE-ε4 allele—the most common gene variant linked with late onset of the disease. And more-recent studies suggest exercise can combat brain deterioration associated with the disease.

Studying exercise’s effect on the nervous system could help researchers identify the best and most efficient strategy to maintain brain health as we age.—Giselle Petzinger, University of Southern California

In 2018, van Praag, along with researchers from Harvard Medical School, MIT, Massachusetts General Hospital, the Dana-Farber Cancer Institute, and the Salk Institute, published a mouse study that found that neither a neuroprotective drug nor a gene therapy to overproduce WNT3, a protein that has been linked to neurogenesis, reversed signs of dementia. Yet, when the mice were allowed to exercise, their cognitive performance improved. When the team combined the neuroprotective drug with treatments to overexpress the Bdnf gene in the brains of mice that didn’t exercise, improvements in their cognitive performance matched those of the mice that were given access to a running wheel.10 The work, van Praag says, may provide avenues toward treating patients with neurodegenerative diseases who are too frail to exercise.

The result also offers support for the 58 clinical trials currently being done on exercise, cognition, and Alzheimer’s disease. There are nearly 100 ongoing trials, including Petzinger’s, investigating exercise’s role in easing Parkinson’s symptoms, and hundreds more looking at exercise as an intervention against depression. Some researchers are even testing the effects of exercise on aging.

“An active lifestyle is not going to turn a 70-year-old brain into a 30-year-old brain,” says Petzinger. “But studying exercise’s effect on the nervous system could help researchers identify the best and most efficient strategy—whether it’s activity alone or activity paired with drugs—to maintain brain health as we age.”

Researchers untangle the multifarious nature of muscle aging. So far, the only reliable treatment is exercise.

Sep 1, 2018

GILLIAN BUTLER-BROWNE, VINCENT MOULY, ANNE BIGOT, CAPUCINE TROLLET

To you readers over age 30, we’ve got some bad news for you. Chances are good you’ve already begun losing muscle. And it only gets worse. Up to a quarter of adults over the age of 60 and half of those over 80 have thinner arms and legs than they did in their youth.

In 1988, Tufts University’s Irwin Rosenberg coined the term “sarcopenia” from Greek roots to describe this age-related lack (penia) of flesh (sarx). Muscle aging likely has several underlying factors, including decreased numbers of muscle stem cells, mitochondrial dysfunction, a decline in protein quality and turnover, and hormonal deregulation. Loss of muscle mass is associated with—and possibly preceded by—muscle weakness, which can make carrying out daily activities, such as climbing stairs or even getting up from a chair, difficult for many seniors. This can lead to inactivity, which itself leads to muscle loss at any age. Thus, older people can enter a vicious cycle that will eventually lead to an increased risk of falls, a loss of independence, and even premature death.

The good news is that exercise can stave off and even reverse muscle loss and weakness. Recent research has demonstrated that physical activity can promote mitochondrial health, increase protein turnover, and restore levels of signaling molecules involved in muscle function. But while scientists know a lot about what goes wrong in aging, and know that exercise can slow the inevitable, the details of this relationship are just starting to come into focus.

The role of muscle stem cells

Skeletal muscle consists of multinucleated fibers formed by the fusion of muscle precursor cells, or myoblasts, during embryonic and fetal development and postnatally until the tissue reaches its adult size. Mature fibers are post-mitotic, meaning they do not divide anymore. As a result, in adulthood both muscle growth and repair are made possible only by the presence of muscle stem cells.

In 1961, Rockefeller University biophysicist Alexander Mauro, using electron microscopy, first described muscle stem cells, calling them “satellite cells” because of their position at the periphery of the muscle fiber.1Subsequently, researchers have demonstrated that satellite cells are the only cells able to repair muscle—which explains why recovery from muscle injuries among the elderly is slow and often incomplete: the number of satellite cells falls from 8 percent of total muscle nuclei in young adults to just 0.8 percent after about 70 to 75 years of age.

Of course, a decline of the satellite cells’ ability to divide and repair could also be to blame, but research does not support this idea. In pioneering studies carried out in 1989, biologists Bruce Carlson and John Faulknerat the University of Michigan showed that muscle isolated from a two-year-old rat was repaired faster and better when grafted into two- to three-month-old rats.2 More recently, we isolated these cells from young and old adults and were surprised to find that elderly human satellite cells grew in culture as well as those from young subjects did.3

The elderly human satellite cells we examined did, however, show dramatic changes in their epigenetic fingerprint, with the repression of many genes by DNA methylation. One gene, called sprouty 1, is known to be an important regulator of cell quiescence. Reduced sprouty 1 expression can limit satellite cell self-renewal and may partially explain the progressive decline in the number of satellite cells observed in human muscles during aging. Indeed, stimulation ofsprouty 1 expression prevents age-related loss of satellite cells and counteracts age-related degeneration of neuromuscular junctions in mice.4

Mitochondrial contributors

Other likely culprits of muscle aging are the mitochondria, the powerhouses of muscle. To work efficiently, skeletal muscle needs a sufficient number of fully functional mitochondria. These organelles represent around 5 percent to 12 percent of the volume of human muscle fibers, depending on activity and muscle specialization (fast-twitch versus slow-twitch). And research suggests that abnormalities in mitochondrial morphology, number, and function are closely related to the loss of muscle mass observed in the elderly.

In 2013, David Glass of Novartis and colleagues found that markers of mitochondrial metabolism pathways were significantly downregulated as rats aged, and this correlated with the onset of sarcopenia.5 Although the findings are merely correlative, the timing and near-perfect relationship between decline in mitochondrial gene expression and the onset of sarcopenia provides strong evidence that mitochondrial dysfunction may be driving sarcopenia. The expression of genes and production of proteins that regulate mitochondrial fission and fusion—processes that maintain mitochondrial volume and function—also dropped, suggesting that mitochondrial dynamics are also perturbed during muscle aging.

As with muscle stem cell decline, the underlying cause of poor mitochondrial health may be gene regulation. In 2016, Alice Pannérec and her colleagues from Nestlé Institute of Health Sciences and Manchester Metropolitan University in the UK examined the transcriptomes of rat and human muscle and found that susceptibility to sarcopenia in both species was closely linked to deregulation of gene networks involved in mitochondrial processes, regulation of the extracellular matrix, and fibrosis, the formation of excess connective tissue in a muscle caused by the accumulation of extracellular matrix proteins.6

Protein quality control

Even if they eat plenty of protein, older people often cannot maintain muscle mass, probably because their bodies cannot turn proteins into muscle fast enough to keep up with the natural rate of the tissue’s breakdown. Moreover, the muscles of older people undergo lower levels of autophagy, a process that under healthy conditions recycles used and damaged proteins, organelles, and other cell structures. This can result in an imbalance between protein production and degradation that is likely linked to muscle aging.

There may also be other ways that reduced autophagy may contribute to both muscle loss and muscle weakness during aging. In order to maintain muscle strength, muscle cells must get rid of the intracellular garbage that accumulates over time. In the case of muscle cells, this garbage includes old organelles such as mitochondria and endoplasmic reticuli, clumps of damaged proteins, and free radicals, all of which can become cytotoxic over time. By recycling mitochondria, muscle fibers boost energy production and preserve muscle function. If muscle fibers fail to clear these potentially dangerous entities, they will become smaller and weaker. Sure enough, in a study from Marco Sandri’s group at the University of Padova in Italy, mice whose skeletal muscles lacked one of the main genes that controls autophagy, Atg7, had profound muscle loss and age-dependant muscle weakness.7

Blood signals

In 2005, Stanford University stem cell biologist Thomas Rando and colleagues combined the circulation of young and old mice and found that factors in the blood of young mice were able to rejuvenate muscle repairin aged mice. It is now well known that the levels of circulating hormones and growth factors drastically decrease with age and that this has an effect on muscle aging. Indeed, hormone replacement therapy can efficiently reverse muscle aging, in part by activating pathways involved in protein synthesis.

Moreover, the muscle itself is a secretory endocrine organ. Proteins produced by the muscle when it contracts flow into the blood, either on their own or encased in membrane-bound vesicles that protect them from degradation by circulating enzymes. Bente Pedersen of the Centre of Inflammation and Metabolism and Centre for Physical Activity Research in Denmark was the first to use the term myokine to describe these proteins. Secreted myokines can act locally on muscle cells or other types of cells such as fibroblasts and inflammatory cells to coordinate muscle physiology and repair, or they can have effects in distant organs, such as the brain.

Although several of these myokines have been identified—in culture, human muscle fibers secrete up to 965 different proteins—researchers have only just begun to understand their role in muscle aging. The first myokine to be identified, interleukin-6 (IL-6), participates in muscle maintenance by decreasing levels of inflammatory cytokines in the muscle environment, while increasing insulin-stimulated glucose uptake and fatty-acid oxidation. Elderly people with high circulating levels of IL-6 are more prone to sarcopenia. Another myokine, insulin-like growth factor 1 (IGF-1), can trigger the swelling of muscle fibers, including after exercise. IGF-1 levels decrease with age, as do levels of the cell-surface receptor that IGF-1 binds to, and mice that overexpress IGF-1 are resistant to age-related sarcopenia.Nathalie Viguerie and colleagues from the Institute of Metabolic and Cardiovascular Diseases at INSERM-Toulouse University in France recently discovered a novel myokine, which they termed apelin.8 The researchers have demonstrated that this peptide can correct many of the pathways that are deregulated in aging muscle. When injected into old mice, apelin boosted the formation of new mitochondria, stimulated protein synthesis, autophagy, and other key metabolic pathways, and enhanced the regenerative capacity of aging muscle by increasing the number and function of satellite cells. As with IGF-1, levels of circulating apelin declined during aging in humans, suggesting that restoring apelin levels to those measured in young adults may ameliorate sarcopenia.

Exercise to combat muscle aging

Although the causes of muscle loss are numerous and complex, there is now copious evidence to suggest that exercise may prevent or reverse many of these age-related changes, whereas inactivity will accelerate muscle aging. Earlier this year, for example, Janet Lord of the University of Birmingham and Steven Harridge at King’s College London examined the muscles of 125 male and female amateur cyclists and showed that a lifetime of regular exercise can slow down muscle aging: there were no losses in muscle mass or muscle strength among those who were older and exercised regularly. More surprisingly, the immune system had not aged much either.9

Exercise’s influence on muscle health likely acts through as many mechanisms as those underlying age-related muscle loss and weakness. For example, the number of satellite cells can be increased by exercise, and active elderly people have more of these cells than more-sedentary individuals do. This is the reason why exercise prior to hip and knee surgery can speed up recovery in the elderly.

Physical activity also affects the muscle’s mitochondria. A lack of exercise decreases the efficiency and number of mitochondria in skeletal muscle, while exercise promotes mitochondrial health. Last year, Caterina Tezze in Sandri’s lab at the University of Padova identified a strong correlation between a decline in the levels of OPA1, a protein involved in shaping the mitochondria, and a decrease in muscle mass and force in elderly subjects, while OPA1 levels were maintained in the muscles of senior athletes who had exercised regularly throughout their lives.10

Age-related muscle diseases

Sarcopenia is part of the general process of aging, but it can be triggered prematurely in some late-onset muscle diseases. For example, oculopharyngeal muscular dystrophy (OPMD) is a rare genetic disease that primarily affects the eyelid (oculo) and throat (pharyngeal) muscles. Mutations in the polyadenylate binding protein nuclear 1 (PABPN1) gene lead to the production of an abnormal protein that forms aggregates only in nuclei of muscle fibers. The late onset of the disease, which generally appears between 50 and 60 years of age, suggests that the affected muscles successfully cope with the abnormal protein for many years. However, the ability to deal with abnormal proteins decreases with age, and an imbalance between elimination and aggregation could trigger the onset of OPMD.

OPMD shows mechanistic similarities with severe degenerative disorders in which perturbed RNA metabolism and pathological assemblies of RNA-binding proteins are involved in the formation of cytoplasmic or nuclear aggregates. In patients with spinocerebellar ataxias, ALS, Alzheimer’s, Huntington’s, or Parkinson’s diseases, these aggregates form in the neurons. In the case of myotonic dystrophy and inclusion body myositis, they form in the muscle fibers. Defining the exact alteration in RNA metabolism is an interesting question facing researchers studying muscle aging. Of note, all of these diseases are also characterized by abnormal mitochondria, which are observed in aging muscle.

Research into these diseases should not only lead to specific treatments, but also to interventions for the generally healthy aging population. And the reverse is also true: understanding how to stall muscle aging may provide tools to ameliorate pathological conditions. Therefore, cooperation between the pathophysiology and aging fields to study these diseases, for which animal and cellular models exist, should be a focus of future research.

Exercise can even spur muscle cells to maintain more-youthful levels of gene transcripts and proteins. For example, Sreekumaran Nair from the Mayo Clinic in Rochester, Minnesota, and colleagues found that high-intensity aerobic interval training reversed many age-related differences in muscle composition, including restoring mitochondrial protein levels.11 And Simon Melov at the Buck Institute for Research on Aging and Mark Tarnopolsky of McMaster University in Canada and their colleagues have found that while healthy older adults (average age 70) had a gene-expression profile that was consistent with mitochondrial dysfunction prior to a resistance exercise training program, in just six months this genetic fingerprint had completely reversed to expression levels comparable to those observed in young subjects. Additionally, exercise improved muscle function: the older adults were 59 percent weaker than the younger adults before training, and only 38 percent weaker afterward.12 Different types of exercise can trigger variable but specific responses in the muscle. For example, whereas strength training is efficient at making muscle, high intensity interval training in aerobic exercises such as biking and walking had the greatest effect at the cellular level at combating age-related loss and weakness, according to Nair’s work.

Exercise may prevent or reverse many of these age-related changes, whereas inactivity will accelerate muscle aging.

Exercise also appears to influence autophagy. In December 2011, Sandri and his colleagues were the first to report, in mice, that autophagy activity could be boosted by voluntary physical activity, in this case, running on a treadmill.13 In January 2012, the team of Beth Levine at the University of Texas Southwestern Medical Center confirmed that exercise rapidly increased autophagy activity and that autophagy is required for exercise to have its beneficial effects: physically active mice that were unable to ramp up autophagy did not show any increase in muscle mass, mitochondrial content, or insulin sensitivity after running.14

Finally, exercise can also apparently restore levels of myokines that decline with age. For example, when elderly subjects followed a regular program of physical activity, there was a direct correlation between the improvement in their physical performance and the increase in the level of circulating apelin.15Similarly, Ivan Bautmans from Vrije Universiteit Brussel showed that increased circulating levels of inflammation markers correlate with muscle fatigue in geriatric patients, and that resistance training decreased inflammatory myokines in young adults.16

By these mechanisms and others we have yet to discover, exercise can improve overall strength in the elderly, and specifically, the metabolic vigor of skeletal muscle. Being the most abundant tissue in the average human body, accounting for 30 percent to 40 percent of its total mass, muscle is not only critical for locomotion and breathing, but also for glucose, lipid, and amino-acid homeostasis. The age-associated loss of muscle mass and quality thus contributes to the general metabolic dysfunction commonly seen in elderly patients. In older women, one hour of brisk walking produced elevated insulin sensitivity on the following day.17 Therefore, it is never too late to exercise to try to combat the consequences of muscle aging.

A detailed understanding of the molecular and cellular pathways involved in muscle aging could pave the way for the development of therapeutic interventions to boost protein synthesis and increase muscle mass. For now, regular exercise combined with good nutrition is still the most effective way to fight sarcopenia, and possibly aging overall. In addition to detailing the underlying causes of muscle aging, future research should seek to define optimal physical exercise and nutritional programs to combat age-related muscle loss and weakness. It may not significantly increase human lifespan, but it will certainly help people reach the end of their lifespan in a healthier condition.

Correction (September 4): The original version of this story incorrectly stated that John Faulkner worked with Heather Carlson at the University of Michigan in the late 1980s. Rather, Bruce Carlson was Faulkner’s collaborator. In addition, the online version showed an image of smooth muscle. This has been replaced with one of skeletal muscle to more accurately reflect the content of the article. Finally, a misleading sentence about the role of satellite cells in muscle aging has been removed. Both the number and function of satellite cells likely plays a role in muscle decline. The Scientist regrets the errors.